This latest instalment of our ‘Ask the Experts’ column – with Karl Frontzek (University of Zurich, Switzerland), Herbert Budka (University of Zurich, Switzerland), Marc Diamond (University of Texas Southwestern, TX, USA) and Masahito Yamada (Kanazawa University, Japan) – focuses on the question, ‘Is Alzheimer’s disease transmissible?’. Yesterday we explored the subject of transmissible neurological disorders, and today we focus specifically on the evidence for and against the suggestion that Alzheimer’s disease could be transmissible.

What current evidence is there for Alzheimer’s disease being a transmissible disease? How could it be transmitted?

MD: Both tau and amyloid-beta fibrils can be inoculated into animals to create disease. There is no evidence that Alzheimer’s disease (AD) is initiated in one individual through exposure to material from another afflicted individual.

“For the past few years scientific data has been accumulating indicating ‘prion-like’ or ‘prionoid’ features of Alzheimer’s disease – both for tau protein and beta-amyloid.” – Karl Frontzek

KF: AD is defined through its two hallmark misfolded proteins, namely beta-amyloid and tau protein. For the past few years scientific data has been accumulating indicating ‘prion-like’ or ‘prionoid’ features of AD – both for tau protein and beta-amyloid.

Several groups have isolated aggregated beta-amyloid plaques from human AD patients and inoculated them into mice (that unfortunately were in a lot of cases on a genetic AD background making it hard for these studies to claim true prion properties of beta-amyloid or tau since the mice would have developed AD eventually). Nonetheless, what they could see was the de novo or accelerated formation of plaques (for beta-amyloid) or tangles (for tau protein).

In 2015, a study in Nature by Sebastian Brandner (University College London, UK) and colleagues made a big splash about the transmissibility of AD. They investigated the brains from patients receiving growth hormone (GH) preparations that were already known to be contaminated with Creutzfeldt Jakob Disease (CJD) prions. Unexpectedly, they discovered that these GH recipients suffered from AD at a very young age, as well as that beta-amyloid was accumulating in the pituitary glands of AD patients – pituitary glands comprising the source of GH preparations.

At the beginning of this year our lab worked in cooperation with the Medical University of Vienna (Austria) on a study that indicated that in young patients who received CJD-contaminated cadaveric dural grafts, a lot of concomitant AD pathology could be observed [1] – adding to the observations of Brandner and coworkers.

Gabor Kovacs from the Medical University of Vienna has further analyzed these dural grafted brains [2] and highlighted a close correlation of dural patches and brain beta-amyloid pathology. Transmission could be achieved through seeded propagation of contaminated dural grafts, growth hormone preparations etc. although more research has to be performed.

How do amyloid-beta proteins, the pathological hallmark of AD, compare functionally to known prion proteins?

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